H. Marshall et al., LACK OF C-JUN EXPRESSION IN A TRANSFORMED-CELL LINE ISOLATED BY GLUCOCORTICOID PROMOTION OF RAS-TRANSFECTED RAT EMBRYO FIBROBLASTS, Oncogene, 8(5), 1993, pp. 1303-1309
Rat embryo fibroblasts (REFs) are inefficiently transformed by the T24
-ras oncogene. A contributing factor to cellular resistance to transfo
rmation is the limited tolerance to p21-ras oncoprotein expression. He
re we present data suggesting that long-term glucocorticoid treatment
of ras oncogene-transfected REFs results in increased tolerance to p21
-ras oncoproteins, leading to expression of the transformed phenotype.
Stably transformed cell lines that expressed high levels of H-ras and
could be maintained in the absence of hormone were isolated. In three
out of four tines studied, the AP-1-dependent collagenase gene was ex
pressed at a low level. In one of these lines, low collagenase express
ion was paralleled by lack of c-jun mRNA. Immunochemical analysis reve
aled that progression to hormone independence was not paralleled by mu
tations in the p53 gene. We propose that a decreased expression of AP-
1-driven genes may result in increased tolerance to p21-ras oncoprotei
n.